Siyao Li

First Hospital of China Medical University

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Xiaoru Hu

Second Xiangya Hospital of Central South University

Zheng Dong

Charlie Norwood VA Medical Center

Zining Zhang

First Hospital of China Medical University

Qingqing Wei

Augusta University

Yajing Fu

China Medical University

Michael T. Heneka

German Center for Neurodegenerative Diseases

Emrah Düzel

German Center for Neurodegenerative Diseases

Annika Spottke

University of Bonn

Christoph Laske

Hertie Institute for Clinical Brain Research

Frank Jessen

University of Cologne

Cooperative Institutions

Northeast Agricultural University

German Center for Neurodegenerative Diseases

Chinese Academy of Sciences

Central South University

Chinese Academy of Medical Sciences & Peking Union Medical College

Jilin University

Charité - Universitätsmedizin Berlin

Sun Yat-sen University

Humboldt-Universität zu Berlin

Peking University

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Central neurocytoma: Radiological and clinico-pathological findings in 18 patients and one additional MRS case

Journal of Neuroradiology (2013)

Haleena Ramsahye Huijin He Xiaoyuan Feng Siyao Li Ji Xiong

Central neurocytoma

10.1016/j.neurad.2012.05.007

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Citations (20)

A panel of autoantibodies as potential early diagnostic serum biomarkers in patients with cervical cancer

Tumor Biology (2016)

Mingmei Huangfu Shuang Xu Siyao Li Baosheng Sun Kuang-Hui Lee

The study was designed to test whether circulating autoantibodies against associated antigens (TAAs) were altered in early cervical cancer and benign cervical tumors. A total of 111 cervical cancer patients, 137 cervical benign tumor patients, and 160 healthy volunteers matched in age were recruited in this study. The expression of autoantibodies was tested using in-house developed enzyme-linked immunosorbent assay (ELISA) with linear peptide envelope antigens derived from TAAs. One-way ANOVA test showed that there was no difference in the CD25 autoantibody expression among the cervical cancer group, benign tumor group, and healthy control group (P = 0.063; P = 0.191). The expression of autoantibodies against survivin and TP53 in the cervical cancer group was significantly higher than that in the benign tumor group (P < 0.001; P < 0.001). The levels of autoantibodies against cyclinB-1 and ANXA-1 were higher in the cervical cancer group than in the healthy control group (P = 0.010; P = 0.001), while autoantibodies in the cervical cancer group showed no difference in expression compared with that in the benign tumor group. The panel of five TAAs showed a sensitivity of 37.8 % and a specificity of 90 %, which was much higher than the sensitivity of the single-TAA testing group. The data from this study further support our previous hypothesis that the detection of autoantibodies for the diagnosis of a specific cancer type can be enhanced using a panel of several selected TAAs as target antigens.

10.1007/s13277-015-4472-1

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J-shaped association of free triiodothyronine to free thyroxine ratio with 5-year mortality among patients with chronic kidney disease: a prospective cohort study

International Urology and Nephrology (2023)

Siyao Li Mengru Zeng

Nephrology

10.1007/s11255-023-03548-7

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Additional file 2 of Transcriptional insights into the CD8+ T cell response in mono-HIV and HCV infection

Figshare (2020)

Siyao Li Zining Zhang Yongjun Jiang Yajing Fu Hong Shang

Additional file 2. CD8+ T cell DEGs from HIV chronic progressors compared with healthy donors

10.6084/m9.figshare.11895516

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p53 in Proximal Tubules Mediates Chronic Kidney Problems after Cisplatin Treatment

Cells (2022)

Shuangshuang Fu Xiaoru Hu Zhengwei Ma Qingqing Wei Xiaohong Xiang

Nephrotoxicity is a major side-effect of cisplatin in chemotherapy, which can occur acutely or progress into chronic kidney disease (CKD). The protein p53 plays an important role in acute kidney injury induced by cisplatin, but its involvement in CKD following cisplatin exposure is unclear. Here, we address this question by using experimental models of repeated low-dose cisplatin (RLDC) treatment. In mouse proximal tubular BUMPT cells, RLDC treatment induced p53 activation, apoptosis, and fibrotic changes, which were suppressed by pifithrin-α, a pharmacologic inhibitor of p53. In vivo, chronic kidney problems following RLDC treatment were ameliorated in proximal tubule-specific p53-knockout mice (PT-p53-KO mice). Compared with wild-type littermates, PT-p53-KO mice showed less renal damage (KIM-1 positive area: 0.97% vs. 2.5%), less tubular degeneration (LTL positive area: 15.97% vs. 10.54%), and increased proliferation (Ki67 positive area: 2.42% vs. 0.45%), resulting in better renal function after RLDC treatment. Together, these results indicate that p53 in proximal tubular cells contributes significantly to the development of chronic kidney problems following cisplatin chemotherapy.

Nephrotoxicity

Knockout mouse

10.3390/cells11040712

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WY14643, a agonist of PPARα, attenuates HFD-induced AIH by regulating hepatocyte lipid metabolism, necrosis and apoptosis via inhibiting JNK signaling pathway

Research Square (Research Square) (2023)

Cuijuan Zhao Xingliang Zhao Guixian Ji Siyao Li Zhou Lü

Abstract Aim of the study : The regulation molecular mechanism of the occurrence and development of AIH by PPARα and JNK signaling pathway. Methods : Mice were fed for 16 weeks either on a normal chow diet (ND) consisting of 4.5% fat or a HFD. Mice were intravenously administered Con A (20 mg/kg) to induce the AIH. GW6471 (20 mg/kg) or WY14643 (6 mg/kg) was injected intraperitoneally for 3days. The mice and liver and spleen tissues were weighted. The histopathological analysis was performed by HE staining. The Inflammatory factors IL-1β, IL-6 and TNF-α was detected using ELISA assay. The mRNA and protein levels were detected using RT-qPCR and Western blotting. Results : HFD could significantly exacerbate the ConA-induced AIH, including liver steatosis, fat accumulation and liver inflammation of mice. Compared with other groups, necroptosis formation and apoptosis-related proteins, which were expressed at abnormally high levels in the liver tissues of HFD + ConA group, were significantly up-regulated by HFD treatment. Therefore, HFD could promote the programmed necrosis and apoptosis in AIH mice. At the same time, HFD could inhibit the expression of PPARα and activate the JNK signaling pathway in AIH mice. Furthermore, PPARα inhibitor GW6471 could further aggravate the necrosis and apoptosis of AIH mice and PPARα agonist WY14643 could alleviate the deterioration of HFD in AIH mice. Importantly, PPARα agonist WY14643 could further alleviate the necrosis and apoptosis of AIH mice through inhibiting the JNK signaling pathway. Conclusion : Our findings demonstrated that PPARα had the efficacy on inhibiting HFD-induced AIH progression by inhibiting the necrosis and apoptosis of hepatocyte and the lipid metabolism abnormity of liver. Further molecular mechanism study found that WY14643 could upregulate the PPARα and inhibit the function of activating JNK signaling pathway.

Steatosis

10.21203/rs.3.rs-3002358/v1

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Cellular Senescence in Repeated Low-Dose Repeated Cisplatin-Induced CKD

Journal of the American Society of Nephrology (2022)

Siyao Li Man J. Livingston Zheng Dong

Senescence

Repeated measures design

10.1681/asn.20223311s1587c

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Pseudogene identification pipeline

Figshare (2020)

Chu Xiao Siyao Li Sishuo Wang

This is a manually modified pipeline based on the program suite Psi-Phi (Lerat and Ochman, 2004), which identifies pseudogenes by doing tblastn within a cluster of closely related genomes.
Input data
1. Amino acid files of all genomes named *.faa2. Genome fasta files named *.fasta (draft genome) or *.fas (complete genome)3. Genbank files of all genomes named *.gbk
Original Psi-Phi scripts are designed for complete genome. For genome assemblies that have not been completely assembled into a single chromosome, all contigs of a genome should be concatenated to an artificially assembled genome first (*.fasta->*.fas) as the input of Psi-Phi.
Instructions for pseudogene identification (Psi-Phi)
1. Makeblastdb for tblastn
In this step, command line will be written as below to make nucleotide database of all artificially assembled genome.
makeblastdb -in input.fas -dbtype nucl -parse_seqids -out input.fas
2. Run tblastn jobs
In this step, command line will be written as below to submit blast jobs for all pairs of the genome sequences.
tblastn -query query.faa -db target.fas -outfmt 6 -evalue 1e-15 -out query.vs.target.blast
3. Batch run module1 of Psi-Phi using batch.module1.pl
This step retrieves particular data from a blast file, output results will be found in 'query.vs.target.sortie.out' files.
4. Batch run module2 of Psi-Phi using batch.module2.pl
This step determines the list and category of each pseudogene candidate using the output of the first module. Potential pseudogenes will be found in 'pseudo_target_use_query' files.
Instructions for pseudogene filtering
The filtering step is further applied to filter out misidentified pseudogenes by Psi-Phi.
Citation
If you are interested in using this modified pipeline for pseudogene identification with filtering, please cite:
Lerat E, Ochman H. Ψ-Φ: Exploring the outer limits of bacterial pseudogenes. Genome Res 2004; 14: 2273–2278.

Chu X, Li S, Wang S, Luo D, Luo H. Gene Loss through Pseudogenization Contributes to the Ecological Diversification of a Generalist Roseobacter Lineage. (unpublished)

Pseudogene

Identification

10.6084/m9.figshare.12545984

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Associations of Ureaplasma urealyticum infection with male infertility and intrauterine insemination outcomes

Asian Journal of Andrology (2024)

Yangyang Wan Xiaoyun Shi Wenjing Liu Shun Bai Xin Chen

Ureaplasma urealyticum (UU) is one of the most commonly occurring pathogens associated with genital tract infections in infertile males, but the impact of seminal UU infection in semen on intrauterine insemination (IUI) outcomes is poorly understood. We collected data from 245 infertile couples who underwent IUI at The First Affiliated Hospital of USTC (Hefei, China) between January 2021 and January 2023. The subjects were classified into two groups according to their UU infection status: the UU-positive group and the UU-negative group. We compared semen parameters, pregnancy outcomes, and neonatal birth outcomes to investigate the impact of UU infection on IUI outcomes. There were no significantly statistical differences in various semen parameters, including semen volume, sperm concentration, total and progressive motility, sperm morphology, leukocyte count, the presence of anti-sperm antibody, and sperm DNA fragmentation index (DFI), between the UU-positive and UU-negative groups of male infertile patients (all P > 0.05). However, the high DNA stainability (HDS) status of sperm differed between the UU-positive and UU-negative groups, suggesting that seminal UU infection may affect sperm nuclear maturation (P = 0.04). Additionally, there were no significant differences in pregnancy or neonatal birth outcomes between the two groups (all P > 0.05). These results suggest that IUI remains a viable and cost-effective option for infertile couples with UU infection who are facing infertility issues.

Ureaplasma urealyticum

Intrauterine insemination

Donor insemination

Ureaplasma

10.4103/aja202489

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LncRNA AK154753 promotes acute kidney ischemia-reperfusion injury via modulating the miR-345-3p/Bak and miR-708-5p/Bim axes

Research Square (Research Square) (2022)

Yunzhen Deng Yi He Kaiting Zhuang Jing Xi Siyao Li

Abstract Acute kidney injury (AKI) is one of a complex clinical syndrome with various causes and poor efficacy. The pathophysiology of AKI includes inflammation, cell apoptosis and cell death. Long noncoding RNAs (lncRNAs) represent a class of functional RNA molecules with a length of more than 200 nucleotide units (NT) and no ability to encode proteins. To identify novel molecular mechanism and potential targets for AKI, the differential expressed lncRNAs between normal and AKI tissues were analyzed with bioinformatics tool. In the present study, the mouse kidney ischemia/reperfusion injury (IRI) model and cell oxygen and glucose deprivation/ reperfusion (OGD/R) model were established. The expression levels of lncRNAs, miRNAs and mRNAs were detected by high-throughput sequencing technology. Meanwhile, lncRNA, miRNA expression levels were detected by quantitative real-time PCR. Luciferase analysis was used to further investigate the interaction between lncRNA AK154753 and miRNA, miRNA and mRNA. Western-blot were performed to test the expression of apoptosis related proteins. Furthermore, TUNEL assay was united with flow cytometry to detect cell apoptosis rate. We found lncRNA AK154753 was significantly up-regulated, while miR-345-3p and miR-708-5p were significantly down-regulated during IRI. At the same time, IRI triggered cell apoptosis both in vivo and in vitro as the evidence by upregulation of Bim/Bak/cleaved-caspase3. Luciferase analysis showed that lncRNA AK154753 could both interacted with miR-345-3p and miR-708-5p, miR-345-3p could interacted with Bak, miR-708-5p could interacted with Bim respectively. Inhibition of lncRNA AK154753 alleviated cell apoptosis along with miR-345-3p/miR-708-5p up-regulated during IRI. In conclusion, the results suggest that lncRNA AK154753 participates in the occurrence and development of acute kidney ischemia-reperfusion injury by regulating miR-345-3p/Bak, miR-708-5p/Bim axes. Inhibiting lncRNA AK154753 may represent new therapeutic modalities for renal IR injury.

10.21203/rs.3.rs-1770222/v1

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